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Biomedical subjects

W B White

Publications and source records attributed to W B White.

At least 145 records · Page 8Linked to original sources
PubMed1986

Improved left ventricular filling accompanies reduced left ventricular mass during therapy of essential hypertension.

Abnormal left ventricular diastolic performance, an early manifestation of hypertension in the heart, may precede the development of left ventricular hypertrophy. To assess effects of antihypertensive therapy on the heart, left ventricular mass (determined by echocardiography) and rapid left ventricular filling rate (determined by radionuclide ventriculography) were compared before and after 6 months of treatment of 16 patients. Nitrendipine (a dihydropyridine calcium channel blocker) was given alone or in combination with either propranolol or hydrochlorothiazide, or both, and significantly reduced blood pressure (156/103 +/- 12/7 to 137/89 +/- 10/6 mm Hg). In 6 of the 16 patients, left ventricular mass decreased by more than 10% (270 +/- 95 to 193 +/- 47 g, p less than 0.01); in the same patients, left ventricular filling rate increased (2.03 +/- 0.35 to 2.30 +/- 0.45 end-diastolic counts/s [EDC/s], p less than 0.01). In the one patient whose left ventricular mass increased (137 to 195 g), left ventricular filling rate decreased from 2.01 to 1.78 EDC/s. In the remaining nine patients who had no change in left ventricular mass, there was no significant changes in left ventricular filling. The changes in ventricular mass and filling could not be related to the extent of change in blood pressure or heart rate. These data suggest that regression of left ventricular mass during antihypertensive therapy with nitrendipine is accompanied by improved diastolic function.

Adult↗
PubMed1986

Effects of chronic cetamolol therapy on resting, ambulatory, and exercise blood pressure and heart rate.

We studied blood pressure (BP) and heart rate (HR) responses in 12 patients with hypertension who were receiving cetamolol, a cardioselective beta-blocker with intrinsic sympathomimetic activity. The BP and HR parameters were evaluated at rest (casual, office readings), with ambulatory BP monitoring, and after treadmill exercise testing. At a mean (+/- SD) dose of 46 +/- 21 mg/day, casual supine BP decreased by 10/12 mm Hg (P less than 0.05 for systolic; P less than 0.01 for diastolic) compared with placebo, while HR decreased 4 bpm. Cetamolol resulted in a significant reduction in the mean 24-hour systolic BP. The most striking reduction occurred in the BP at work (23 mm Hg), with almost no decrease in the BP during sleep. Ambulatory HR reductions occurred while the subjects were at work (9 bpm; P less than 0.05) but not while at home (awake) or during sleep. The mean duration of exercise was the same during cetamolol and placebo phases, but both HR and BP fell significantly at peak performance after cetamolol. These data suggest that cetamolol reduces BP without lowering HR at rest. During periods of increased adrenergic activity such as work and dynamic exercise, both HR and BP are reduced.

Acetamides↗
PubMed1986

Effect of the calcium channel blocker nitrendipine on left ventricular mass in patients with hypertension.

Reductions in left ventricular (LV) mass have been reported after antihypertensive therapy with certain sympatholytic agents and converting enzyme inhibitors, but little or no improvement has been noted after vasodilator therapy. In this study we evaluated the effect of the calcium channel blocker nitrendipine on echocardiographic LV mass. During a 12-month period, nitrendipine was used as monotherapy in 30 patients and in combination with propranolol or a diuretic in an additional 28 patients. Nitrendipine monotherapy lowered supine blood pressure from 148/97 to 136/83 mm Hg, but LV mass did not change significantly. Supine blood pressure decreased from 155/103 to 134/86 mm Hg in patients receiving combination therapy but, again, changes in LV mass were not significant. These data suggest that nitrendipine is effective in lowering blood pressure, but this is not associated with a significant decrease in LV mass in patients with mild hypertension.

Adult↗
PubMed1986

Effects of combination therapy with captopril and nifedipine in severe or resistant hypertension.

To assess the effect of potent vasodilator therapy in patients with severe or resistant hypertension, 10 patients underwent therapy with captopril and nifedipine alone and in combination. Blood pressure (BP), heart rate, and blood chemistry values were monitored for 4 weeks during captopril monotherapy and after 8 weeks during combination therapy with captopril and nifedipine. Compared with baseline, the BP decreased during captopril monotherapy (180 +/- 11/98 +/- 7 vs. 209 +/- 16/118 +/- 12 mm Hg; P less than 0.005). After the addition of nifedipine, the BP was further reduced (148 +/- 23/85 +/- 16 mm Hg), but there was no change in heart rate. In three patients not achieving the diastolic BP goal during combination therapy with dosing every 8 hours, automatic 24-hour ambulatory BP monitoring demonstrated lack of antihypertensive control for only the last 2 to 3 hours of the dosing interval. These data demonstrate that combination therapy with captopril and nifedipine is effective in patients with severe hypertension, but frequent dosing intervals are necessary for adequate antihypertensive control.

Adult↗
PubMed1986

Accelerated hypertension associated with the central nervous system toxicity of metrizamide.

A 68-year-old woman with a history of mild hypertension developed a toxic encephalopathy following myelography with metrizamide. Concomitant with the symptoms of vomiting, headache, muscle twitching, and hallucinations was a sudden and marked increase in arterial pressure. Treatment with parenteral vasodilators caused a partial, but transient lowering of the blood pressure. The mental status abnormalities were resolved by treatment with parenteral lorazempam and, subsequently, the blood pressure returned to the premyelography levels. This report demonstrates that metrizamide can induce a severe, accelerated form of hypertension.

Aged↗
PubMed1986

Hypotension with postural syncope secondary to the combination of chlorpromazine and captopril.

A 49-year-old man with severe hypertension and chronic schizophrenia developed marked hypotension with postural syncope following therapy with the combination of chlorpromazine and captopril. Previously, the patient's blood pressure (BP) had been poorly controlled on a regimen of chlorpromazine and hydrochlorothiazide, nadolol, and prazosin. The supine and standing BP and 24-hour ambulatory BP were subsequently studied while the patient was maintained on chlorpromazine and captopril, chlorpromazine alone, and on no therapy. Chlorpromazine alone caused a moderate reduction in supine and standing BP with a reversal of the circadian BP profile. The combination of chlorpromazine and small doses of captopril (12.5 mg/d) induced a reduction in supine BP of 84/32 mm Hg compared with chlorpromazine alone and exaggerated the postural hypotension. Hormonal investigation demonstrated low baseline renin activity that increased during therapy with captopril and a physiologic catecholamine response to change in posture. These data demonstrate that there is a synergism between captopril and chlorpromazine that may result in marked, symptomatic hypotension that is probably unrelated to the baseline level of plasma renin activity or catecholamines.

Blood Pressure↗
PubMed1986

Episodic hypertension secondary to panic disorder.

Episodic elevation of blood pressure was evaluated in two middle-aged men by assessing home, clinic, and 24-hour ambulatory values following exclusion of secondary forms of hypertension. Both individuals had normotensive home and clinic readings. The 24-hour blood pressure was 125/85 +/- 12/9 mm Hg in patient 1 and 119/84 +/- 13/13 mm Hg in patient 2; however, both patients experienced large, sustained rises in blood pressure associated with panic attacks that were not abolished with prophylactic benzodiazepine therapy. Episodic blood pressure elevations were not associated with concomitant increases in heart rate. Patient 1 underwent extensive psychological investigation that diagnosed a panic disorder, and he underwent therapy that reduced the frequency and intensity of his panic-related hypertensive episodes. Because patient 2 demonstrated hypertensive readings at work, he was given a beta-blocking agent that ultimately controlled his blood pressure during episodes of anxiety and panic. These findings suggest that patients with panic attacks may present with episodic hypertension and that ambulatory blood pressure monitoring is useful in the diagnosis of this disorder and in assessment of treatment outcome.

Adult↗
PubMed1986

Assessment of patients with office hypertension by 24-hour noninvasive ambulatory blood pressure monitoring.

To assess the discrepancy between casual (office) and home blood pressure readings in patients performing home blood pressure monitoring, we analyzed office, home, and 24-hour ambulatory blood pressure and heart rates in 19 patients in a prospective four-week study. After the month of study, the average difference between mean office and manual home blood pressures in this office hypertensive group was 30 +/- 17/20 +/- 6 mm Hg. The blood pressures taken in the office were substantially greater than the 24-hour average blood pressures and ambulatory blood pressures during work or while at home (awake). An analysis of the automatic monitor readings while in the doctor's office and at 15-minute intervals after leaving the office showed a progressive reduction in blood pressure and heart rate during the first hour after leaving the office. A mean 24-hour blood pressure of less than 130/80 mm Hg was found in 13 (68%) patients. These data suggest that patients with office hypertension are usually normotensive but may have a persistent and recurrent pressor response in a medical care setting. Ambulatory blood pressure monitoring provides confirmation of not only the office-home disparity, but also suggests that stress other than office visits fails to elicit a hypertensive response.

Ambulatory Care↗
PubMed1985

Modulation of suppressor-cell activity by cimetidine in patients with common variable hypogammaglobulinemia.

Because of evidence of a possible immunoregulatory role for cimetidine, an antagonist to histamine H2 receptors, we studied the effects of this drug in five adult patients with common variable hypogammaglobulinemia. Three patients had excessive suppressor-cell function associated with panhypogammaglobulinemia, whereas the other two had no apparent T-cell defects. The patients were given a one-month course of oral cimetidine (1200 mg daily in four divided doses). Subsequently, the three patients with excessive suppressor-cell function had a marked reduction in suppressor activity along with a decrease in the number of suppressor cells (T8+). One of these three had a marked rise in both in vitro immunoglobulin secretion and serum immunoglobulin concentrations, which was reversible after the drug was stopped for three months and reproducible when therapy with cimetidine was repeated. There was no difference in immunoglobulin secretion or suppressor-cell activity while taking cimetidine between the two patients with common variable hypogammaglobulinemia without excessive suppressor-cell activity and control patients with duodenal ulcers. The data suggest that H2-receptor antagonists may decrease excessive suppressor-cell activity and allow endogenous immunoglobulin production in some patients with common variable hypogammaglobulinemia.

Adult↗
PubMed1985

Erythroderma with spongiotic dermatitis. Association with common variable hypogammaglobulinemia.

Two middle-aged men presented with generalized erythroderma, diffuse alopecia, and hyperkeratosis of the palms and soles. Histopathologic study demonstrated spongiosis (epidermal intercellular edema) with a perivascular lymphohistiocytic infiltrate. Complete immunologic evaluation demonstrated that both patients had panhypogammaglobulinemia and markedly depressed in vitro pokeweed mitogen-induced immunoglobulin secretion. One of the patients also showed poor lymphocyte responses in vitro to T cell mitogens and antigens and had a decreased ratio of helper to suppressor cells. In both patients, the cutaneous lesions improved with systemic corticosteroids, but no significant alteration in the immunologic abnormalities was observed. This report illustrates that chronic erythroderma may be the presenting clinical manifestation of common variable hypogammaglobulinemia.

Agammaglobulinemia↗
PubMed1985

Rapid ventricular filling in left ventricular hypertrophy: II. Pathologic hypertrophy.

To define the extent of left ventricular ejection and filling abnormalities in patients with mild hypertension, a non-imaging nuclear probe was used to generate high resolution time-activity curves in 25 patients with an average systolic blood pressure of 154 +/- 20 mm Hg and diastolic pressure of 98 +/- 8 mm Hg. The hypertensive patients did not meet electrocardiographic criteria for left ventricular hypertrophy, and none had evidence of ischemic or other cardiac disease. Compared with 25 age-matched normal subjects who had average systolic and diastolic pressures of 123 +/- 10 and 79 +/- 8 mm Hg, respectively, the hypertensive patients had a significantly lower ejection rate (2.00 +/- 0.20 versus 2.34 +/- 0.36 end-diastolic counts/s for the control group, p less than 0.05) and ejection fraction (58 +/- 4.9 versus 62 +/- 4.4) (p less than 0.05). The hypertensive patients had a markedly lower average rapid left ventricular filling rate (1.87 +/- 0.32 versus 2.69 +/- 0.41 counts/s for the control group, p less than 0.001). Although there was a modest inverse relation between echocardiographic left ventricular mass index and filling rate in the hypertensive patients (r = -0.59, p less than 0.01), 4 of 12 hypertensive patients with normal left ventricular mass index had a depressed filling rate. All of the hypertensive patients with increased left ventricular mass index had an abnormal left ventricular filling rate (less than 1.89 end-diastolic counts/s).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Effects of chronic nitrendipine on casual (office) and 24-hour ambulatory blood pressure.

To assess the clinical efficacy of chronic nitrendipine therapy in mild to moderate essential hypertension, we studied blood pressure (BP) and heart rate responses in 22 subjects receiving maintenance nitrendipine therapy. Ten subjects (45%) whose hypertension was controlled with chronic monotherapy had an 11/12 mm Hg decrease in supine BP (P less than 0.05) with a mean (+/- SD) dose of 71 +/- 15 mg/day. The 12 (55%) subjects whose hypertension was not controlled with monotherapy had a comparatively higher baseline BP than the other 10 (156/105 +/- 10/6 compared with 150/98 +/- 15/4 mm Hg; P less than 0.05). Eight of the 10 subjects demonstrating office BP control with chronic nitrendipine monotherapy who also had full-time employment underwent continuous ambulatory BP monitoring before and after maintenance monotherapy. Nitrendipine induced a reduction in the mean 24-hour BP and mean BP at home, but did not reduce the BP during work or while asleep. These data suggest that nitrendipine lowers BP when assessed by casual office methods. The ambulatory BP monitor data demonstrate that the hypotensive response to chronic nitrendipine is modified during work periods, which are generally associated with increased adrenergic activity. Ambulatory BP monitoring may be superior to office (casual) monitoring in the assessment of the overall efficacy of antihypertensive drugs.

Adult↗
PubMed1985

Alpha-methyldopa disposition in mothers with hypertension and in their breast-fed infants.

To assess the problem of alpha-methyldopa dosing in lactating mothers with hypertension, we studied three breast-feeding women to determine simultaneous plasma and breast milk concentrations of alpha-methyldopa after a 500 mg oral dose while receiving continuous therapy. Peak excretion of free alpha-methyldopa in breast milk ranged from 0.02 to 1.14 microgram/ml. The breast milk/whole plasma ratios of alpha-methyldopa ranged from 0.19 to 0.34. In two of the three breast-fed infants, plasma levels of alpha-methyldopa were undetectable (less than 0.05 microgram/ml) 6 hours after maternal ingestion of the drug, but in one of these the plasma alpha-methyldopa concentration was 0.09 microgram/ml 10 hours after maternal dosing. It is estimated that when the mother receives 1 gm alpha-methyldopa a day, the maximal cumulative dose of alpha-methyldopa would be 855 micrograms and the average cumulative alpha-methyldopa load to the breast-fed infant would be 195 micrograms, or 0.02% of the maternal dose.

Administration, Oral↗